The present invention relates generally to an implantable cardiac stimulation device. More specifically, the present invention is directed to an implantable cardiac stimulation device with automatic capture verification capabilities made possible during bipolar stimulation by monitoring for the presence of anodal stimulation.
In the normal human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers, causing a depolarization known as a P-wave, and resulting atrial chamber contractions. The excitation pulse is further transmitted to, and through the ventricles via the atrioventricular (A-V) node and a ventricular conduction system, causing a depolarization known as an R-wave and resulting ventricular chamber contractions.
Disruption of this natural pacemaking and conduction system as a result of aging or disease can be successfully treated by artificial cardiac pacing using implantable cardiac stimulation devices, including pacemakers and implantable defibrillators, which deliver rhythmic electrical pulses or anti-arrhythmia therapies to the heart at a desired pacing output (amplitude and pulse width) and rate. A cardiac stimulation device is electrically coupled to the heart by one or more leads possessing one or more electrodes in contact with the heart muscle tissue (myocardium). One or more heart chambers may be electrically stimulated depending on the location and severity of the conduction disorder.
A stimulation pulse delivered to the myocardium must be of sufficient energy to depolarize the tissue, thereby causing a contraction, a condition commonly known as xe2x80x9ccapture.xe2x80x9d In early pacemakers, a fixed, high-output pacing pulse was delivered to ensure capture. While this approach is straightforward, it quickly depletes battery charge and can result in patient discomfort due to extraneous stimulation of surrounding skeletal muscle tissue.
The capture xe2x80x9cthresholdxe2x80x9d is defined as the lowest stimulation pulse output at which capture occurs. By stimulating the heart chambers at, or just above capture threshold, comfortable and effective cardiac stimulation is provided without unnecessary depletion of battery charge. Capture threshold, however, is extremely variable from patient-to-patient due to variations in electrode systems used, electrode positioning, physiological and anatomical variations of the heart itself, and so on. Furthermore, capture threshold will vary over time within a patient as, for example, fibrotic encapsulation of the electrode occurs during the first few weeks after surgery. Fluctuations may even occur over the course of a day or with changes in medical therapy or disease state.
Hence, techniques for monitoring the cardiac activity following delivery of a stimulation pulse have been incorporated in modern pacemakers in order to verify that capture has indeed occurred. If a loss of capture is detected by such capture-verification algorithms, a threshold test is performed by the cardiac pacing device in order to re-determine the threshold and automatically adjust the stimulating pulse output. This approach, called xe2x80x9cautomatic capturexe2x80x9d, improves the cardiac stimulation device performance in at least two ways: 1) by verifying that the stimulation pulse delivered to the patient""s heart has been effective, and 2) significantly increasing the device""s battery longevity by conserving the battery charge used to generate stimulation pulses.
Commonly implemented techniques for verifying capture involve monitoring the intracardiac electrogram (EGM) signals received on the cardiac sensing electrodes. When a stimulation pulse is delivered to the heart, the EGM signals that are manifest concurrent with the depolarization of the myocardium are examined. When capture occurs, detection of an xe2x80x9cevoked response,xe2x80x9d observed as the intracardiac P-wave or R-wave on the EGM, indicates contraction of the respective cardiac tissue. The depolarization of the heart tissue in response to the heart""s natural pacemaking function is referred to as an xe2x80x9cintrinsic responsexe2x80x9d. Through sampling and signal processing algorithms, the presence of an evoked response following a stimulation pulse is determined. For example, if a stimulation pulse is applied to the ventricle, an R-wave sensed by ventricular sensing circuits of the pacemaker immediately following application of the ventricular stimulation pulse evidences capture of the ventricles.
If no evoked response is detected, typically a high-output back-up stimulation pulse is immediately delivered to the heart in order to provide backup support to the patient. An automatic threshold test is next invoked in order to re-determine the minimum pulse output required to capture the heart. An exemplary automatic threshold determination procedure is performed by first increasing the stimulation pulse output level to a relatively high predetermined testing level at which capture is certain to occur. Thereafter the output level is progressively decremented until capture is lost. The stimulation pulse output is then set to a level safely above the lowest output level at which capture was attained. Thus, reliable capture verification is of utmost importance in proper determination of the threshold.
Sensing an evoked response, however, can be difficult for several reasons. The greatest difficulty encountered is probably that of lead polarization. Lead polarization is commonly caused by electrochemical reactions that occur at the lead-tissue interface due to application of an electrical stimulation pulse across the interface. A lead-tissue interface is that point at which an electrode of the pacemaker lead contacts the cardiac tissue. If the evoked response is sensed through the same electrodes through which the stimulation pulses are delivered, the resulting polarization signal, also referred to as xe2x80x9cafterpotentialxe2x80x9d, formed at the electrode can corrupt the evoked response signal that is sensed by the sensing circuits. This undesirable situation occurs often because the polarization signal can be three or more orders of magnitude greater than the evoked response. Furthermore, the lead polarization signal is not easily characterized; it is a complex function of the lead materials, lead geometry, tissue impedance, stimulation output and other variables, many of which are continually changing overtime.
A false positive detection of an evoked response may lead to missed heartbeats, a highly undesirable and potentially life-threatening situation. Failure to detect an evoked response that has actually occurred will cause the pacemaker to unnecessarily invoke the threshold testing function in a chamber of the heart.
The importance of the problem of lead polarization is evident by the numerous approaches that have been proposed for overcoming this problem. For example, specially designed electrodes with properties that reduce the polarization effect have been proposed. When additional electrodes are available for sensing, polarization can be avoided by sensing the EGM signals using a different pair of electrodes than that used for stimulation.
Another problem that prevents reliable evoked response sensing during bipolar stimulation is the presence of anodal stimulation. Typically cathodal stimulation of the myocardium is recommended. Cathodal stimulation produces a negative pulse that acts to reduce the capacitance of the cell membrane allowing depolarization to occur. Anodal stimulation, that is a positive pulse, can also cause cell depolarization by first hyperpolarizing the cell and then, as the cell repolarizes, an overshoot causes depolarization. However, anodal stimulation generally requires higher stimulation output then cathodal stimulation, thus increasing the battery current drain. Anodal stimulation has been thought to increase the risk of arrhythmogenic depolarizations.
During bipolar stimulation, for example using a lead tip electrode as the cathode and a lead ring electrode as the anode, some degree of anodal stimulation may occur at the ring electrode. Anodal stimulation, when it occurs, has been found to change the bipolar evoked response signal morphology. The amplitude of the evoked response signal may be reduced, and the polarity may be reversed. Thus, signal processing algorithms used to recognize a bipolar evoked response signal for the verification of capture may fail to detect an evoked response signal altered due to anodal stimulation. During automatic capture verification, bipolar sensing is normally required to detect an evoked response. Therefore, unipolar stimulation may be required during automatic capture verification in order to reduce the interference of lead polarization and anodal stimulation with evoked response detection.
Bipolar stimulation, however, may be preferred over unipolar stimulation in many patients. Unipolar stimulation interferes with accurate arrhythmia detection in implantable cardioverter defibrillators. The requirement of unipolar stimulation in these devices has excluded the use of automatic capture verification capabilities. While problems of lead polarization can be overcome using low-polarization leads or special output or sensing circuitry, the problem of anodal stimulation preventing the use of automatic capture verification by evoked response detection during bipolar stimulation has not been fully addressed heretofore.
One approach to avoid the problem of lead polarization that would also avoid the problem of anodal stimulation is to detect evidence of the mechanical contraction of the heart chambers by measuring another physiological signal such as blood pressure, blood flow, heart wall motion, or changes in cardiac impedance. However, the use of additional physiological sensors adds cost, more complicated software and hardware requirements, additional implant time and increases reliability issues.
Since the stimulation output at which anodal stimulation begins to occur is generally higher than the cathodal capture threshold, anodal stimulation may not always occur during bipolar stimulation. However, it is a common practice to set stimulation output at a working margin above the cathodal capture threshold to allow for small fluctuations in threshold. Anodal stimulation may therefore occur at varying degrees during bipolar stimulation. Furthermore, the threshold at which anodal stimulation begins to occur is not a definitive value. The probability of anodal stimulation occurring increases with increasing stimulation amplitude.
One way to recognize when anodal stimulation is occurring is by examining the unipolar evoked response signal sensed using the anode electrode, typically a ring electrode, and device housing. When no anodal stimulation is present, a delay of 20 to 40 msec follows the bipolar stimulation pulse prior to the unipolar ring evoked response signal. This delay is thought to be due to the propagation time required for the depolarization wave front to travel from the cathodal stimulation site at the tip electrode to the sensing site at the ring electrode. In contrast, when anodal stimulation is present at the ring electrode, the evoked response immediately follows the stimulation pulse without any delay, and the evoked response signal is altered from the normal evoked response.
It would be desirable, therefore, to provide an implantable cardiac stimulation device capable of performing reliable capture verification during bipolar stimulation by determining when anodal stimulation is present and when it is not present. A method that allows capture detection during bipolar stimulation is needed, which overcomes the problem of anodal stimulation interfering with evoked response detection. Furthermore, it is desirable to implement a method for automatic capture detection during bipolar simulation in a cardiac stimulation device without requiring additional sensors or circuitry components that add cost, current drain and bulk to the system.
The present invention addresses this need by providing an implantable cardiac stimulation device and associated method for detecting when anodal stimulation is occurring during bipolar stimulation and eliminating capture verification based on evoked responses associated with anodal stimulation.
In one embodiment, a method and corresponding device are provided that monitor for anodal stimulation subsequent to a bipolar stimulation. If anodal stimulation is detected, the method and device ignore a detected response for purposes of capture verification. On the other hand, if anodal stimulation is not detected, the method and device perform capture verification based on the detected response.